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A monster called cancer is still one of the most challenging human problems and one of the leading causes of death in the world. Different types of treatment methods are used for cancer therapy; however, there are challenges such as high cost and harmful side effects in using these methods. Recent years have witnessed a surge in the development of therapeutic peptides for a wide range of diseases, notably cancer. Peptides are preferred over antibiotics, radiation therapy, and chemotherapy in the treatment of cancer due to a number of aspects, including flexibility, easy modification, low immunogenicity, and inexpensive cost of production. The use of therapeutic peptides in cancer treatment is a novel and intriguing strategy. These peptides provide excellent prospects for targeted drug delivery because of their high selectivity, specificity, small dimensions, good biocompatibility, and simplicity of modification. Target specificity and minimal toxicity are benefits of therapeutic peptides. Additionally, peptides can be used to design antigens or adjuvants for vaccine development. Here, types of therapeutic peptides for cancer therapy will be discussed, such as peptide-based cancer vaccines and tumor-targeting peptides (TTP) and cell-penetrating peptides (CPP)., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Krüppel-like factor 4 (KLF4), a zinc finger transcription factor, is found in different human tissues and shows diverse regulatory activities in a cell-dependent manner. In the brain, KLF4 controls various neurophysiological and neuropathological processes, and its contribution to various neurological diseases has been widely reported. Parkinson's disease (PD) is an age-related neurodegenerative disease that might have a connection with KLF4. In this review, we discussed the potential implication of KLF4 in fundamental molecular mechanisms of PD, including aberrant proteostasis, neuroinflammation, apoptosis, oxidative stress, and iron overload. The evidence collected herein sheds new light on KLF4-mediated pathways, which manipulation appears to be a promising therapeutic target for PD management. However, there is a gap in the knowledge on this topic, and extended research is required to understand the translational value of the KLF4-oriented therapeutical approach in PD., (© 2023. The Author(s).)

Colistin is used as a last resort for the management of infections caused by multi-drug resistant (MDR) bacteria. However, the use of this antibiotic could lead to different side effects, such as nephrotoxicity, in most patients, and the high prevalence of colistin-resistant strains restricts the use of colistin in the clinical setting. Additionally, colistin could induce resistance through the increased formation of biofilm; biofilm-embedded cells are highly resistant to antibiotics, and as with other antibiotics, colistin is impaired by bacteria in the biofilm community. In this regard, the researchers used combination therapy for the enhancement of colistin activity against bacterial biofilm, especially MDR bacteria. Different antibacterial agents, such as antimicrobial peptides, bacteriophages, natural compounds, antibiotics from different families, N-acetylcysteine, and quorum-sensing inhibitors, showed promising results when combined with colistin. Additionally, the use of different drug platforms could also boost the efficacy of this antibiotic against biofilm. The mentioned colistin-based combination therapy not only could suppress the formation of biofilm but also could destroy the established biofilm. These kinds of treatments also avoided the emergence of colistin-resistant subpopulations, reduced the required dosage of colistin for inhibition of biofilm, and finally enhanced the dosage of this antibiotic at the site of infection. However, the exact interaction of colistin with other antibacterial agents has not been elucidated yet; therefore, further studies are required to identify the precise mechanism underlying the efficient removal of biofilms by colistin-based combination therapy., (© 2023. The Author(s) under exclusive licence to Sociedade Brasileira de Microbiologia.)

Purpose: Diabetes is one of the important and growing diseases in the world. Among the most common diabetic complications are renal adverse effects. The use of apigenin may prevent the development and progression of diabetes-related injuries. The current study aims to review the effects of apigenin in the treatment of diabetic nephropathy., Methods: In this review, a systematic search was performed based on PRISMA guidelines for obtaining all relevant studies on "the effects of apigenin against diabetic nephropathy" in various electronic databases up to September 2022. Ninety-one articles were obtained and screened in accordance with the predefined inclusion and exclusion criteria. Seven eligible articles were finally included in this review., Results: The experimental findings revealed that hyperglycemia led to the decreased cell viability of kidney cells and body weight loss and an increased kidney weight of rats; however, apigenin administration had a reverse effect on these evaluated parameters. It was also found that hyperglycemia could induce alterations in the biochemical and renal function-related parameters as well as histopathological injuries in kidney cells or tissue; in contrast, the apigenin administration could ameliorate the hyperglycemia-induced renal adverse effects., Conclusion: The results indicated that the use of apigenin could mitigate diabetes-induced renal adverse effects, mainly through its antioxidant, anti-apoptotic, and anti-inflammatory activities. Since the findings of this study are based on experimental studies, suggesting the use of apigenin (as a nephroprotective agent) against diabetic nephropathy requires further clinical studies., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

The immune system is the key player in a wide range of responses in normal tissues and tumors to anticancer therapy. Inflammatory and fibrotic responses in normal tissues are the main limitations of chemotherapy, radiotherapy, and also some newer anticancer drugs such as immune checkpoint inhibitors (ICIs). Immune system responses within solid tumors including anti-tumor and tumor-promoting responses can suppress or help tumor growth. Thus, modulation of immune cells and their secretions such as cytokines, growth factors and epigenetic modulators, pro-apoptosis molecules, and some other molecules can be suggested to alleviate side effects in normal tissues and drug-resistance mechanisms in the tumor. Metformin as an anti-diabetes drug has shown intriguing properties such as anti-inflammation, anti-fibrosis, and anticancer effects. Some investigations have uncovered that metformin can ameliorate radiation/chemotherapy toxicity in normal cells and tissues through the modulation of several targets in cells and tissues. These effects of metformin may ameliorate severe inflammatory responses and fibrosis after exposure to ionizing radiation or following treatment with highly toxic chemotherapy drugs. Metformin can suppress the activity of immunosuppressive cells in the tumor through the phosphorylation of AMP-activated protein kinase (AMPK). In addition, metformin may stimulate antigen presentation and maturation of anticancer immune cells, which lead to the induction of anticancer immunity in the tumor. This review aims to explain the detailed mechanisms of normal tissue sparing and tumor suppression during cancer therapy using adjuvant metformin with an emphasis on immune system responses., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Introduction: Although radiotherapy is one of the main cancer treatment modalities, exposing healthy organs/tissues to ionizing radiation during treatment and tumor resistance to ionizing radiation are the chief challenges of radiotherapy that can lead to different adverse effects. It was shown that the combined treatment of radiotherapy and natural bioactive compounds (such as silymarin/silibinin) can alleviate the ionizing radiation-induced adverse side effects and induce synergies between these therapeutic modalities. In the present review, the potential radiosensitization effects of silymarin/silibinin during cancer radiation exposure/radiotherapy were studied., Methods: According to the PRISMA guideline, a systematic search was performed for the identification of relevant studies in different electronic databases of Google Scholar, PubMed, Web of Science, and Scopus up to October 2022. We screened 843 articles in accordance with a predefined set of inclusion and exclusion criteria. Seven studies were finally included in this systematic review., Results: Compared to the control group, the cell survival/proliferation of cancer cells treated with ionizing radiation was considerably less, and silymarin/silibinin administration synergistically increased ionizing radiation-induced cytotoxicity. Furthermore, there was a decrease in the tumor volume, weight, and growth of ionizing radiation-treated mice as compared to the untreated groups, and these diminutions were predominant in those treated with radiotherapy plus silymarin/ silibinin. Furthermore, the irradiation led to a set of biochemical and histopathological changes in tumoral cells/tissues, and the ionizing radiation-induced alterations were synergized following silymarin/silibinin administration (in most cases)., Conclusion: In most cases, silymarin/silibinin administration could sensitize the cancer cells to ionizing radiation through an increase of free radical formation, induction of DNA damage, increase of apoptosis, inhibition of angiogenesis and metastasis, etc. However, suggesting the use of silymarin/silibinin during radiotherapeutic treatment of cancer patients requires further clinical studies., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Purpose: Colorectal cancers are composed of heterogeneous cell populations in the concepts of genetic and functional degrees that among them cancer stem cells are identified with their self-renewal and stemness capability mediating primary tumorigenesis, metastasize, therapeutic resistance, and tumor recurrence. Therefore, understanding the key mechanisms of stemness in colorectal cancer stem cells (CRCSCs) provides opportunities to discover new treatments or improve existing therapeutic regimens., Methods: We review the biological significance of stemness and the results of potential CRCSC-based targeted immunotherapies. Then, we pointed out the barriers to targeting CRCSCs in vivo and highlight new strategies based on synthetic and biogenic nanocarriers for the development of future anti-CRCSC trials., Results: The CSCs' surface markers, antigens, neoantigens, and signaling pathways supportive CRCSCs or immune cells that are interacted with CRCSCs could be targeted by immune monotherapy or in formulation with developed nanocarriers to overcome the resistant mechanisms in immune evader CRCSCs., Conclusion: Identification molecular and cellular cues supporting stemness in CRCSCs and their targeting by nanoimmunotherpy can improve the efficacy of existed therapies or explore novel therapeutic options in future., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Resistance to therapy and the toxicity of normal tissue are the major problems for efficacy associated with chemotherapy and radiotherapy. Drug resistance is responsible for most cases of mortality associated with cancer. Furthermore, their side effects can decrease the quality of life for surviving patients. An enhancement in the tumor response to therapy and alleviation of toxic effects remain unsolved challenges. One of the interesting topics is the administration of agents with low toxicity to protect normal tissues and/or sensitize cancers to chemo/radiotherapy. Melatonin is a natural body hormone that is known as a multitasking molecule. Although it has antioxidant properties, a large number of experiments have uncovered interesting effects of melatonin that can increase the therapeutic efficacy of chemo/radiation therapy. Melatonin can enhance anticancer therapy efficacy through various mechanisms, cells such as the immune system, and modulation of cell cycle and death pathways, tumor suppressor genes, and also through suppression of some drug resistance mediators. However, melatonin may protect normal tissues through the suppression of inflammation, fibrosis, and massive oxidative stress in normal cells and tissues. In this review, we will discuss the distinct effects of melatonin on both tumors and normal tissues. We review how melatonin may enhance radio/chemosensitivity of tumors while protecting normal tissues such as the lung, heart, gastrointestinal system, reproductive system, brain, liver, and kidney., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Aerobic glycolysis, also known as the Warburg effect, is a metabolic phenomenon frequently observed in cancer cells, characterized by the preferential utilization of glucose through glycolysis, even under normal oxygen conditions. This metabolic shift provides cancer cells with a proliferative advantage and supports their survival and growth. While the Warburg effect has been extensively studied, the underlying mechanisms driving this metabolic adaptation in cancer cells remain incompletely understood. In recent years, emerging evidence has suggested a potential link between endoplasmic reticulum (ER) stress and the promotion of aerobic glycolysis in cancer cells. The ER is a vital organelle involved in protein folding, calcium homeostasis, and lipid synthesis. Various cellular stresses, such as hypoxia, nutrient deprivation, and accumulation of misfolded proteins, can lead to ER stress. In response, cells activate the unfolded protein response (UPR) to restore ER homeostasis. However, prolonged or severe ER stress can activate alternative signaling pathways that modulate cellular metabolism, including the promotion of aerobic glycolysis. This review aims to provide an overview of the current understanding regarding the influence of ER stress on aerobic glycolysis in cancer cells to shed light on the complex interplay between ER stress and metabolic alterations in cancer cells. Understanding the intricate relationship between ER stress and the promotion of aerobic glycolysis in cancer cells may provide valuable insights for developing novel therapeutic strategies targeting metabolic vulnerabilities in cancer., Competing Interests: Declaration of Competing Interest We would like to submit a review article entitled “The Role of Endoplasmic Reticulum Stress in Promoting Aerobic Glycolysis in Cancer Cells: An Overview” by Abduladheem Turki Jalil, Mohanad Ali Abdulhadi, Sami Awad Alkubaisy, Sara Hamed Thejeel, Israa M. Essa, Muna S. Merza, Rahman S. Zabibah, Raad Al-Tamimi for possible publication in Pathology – Research and Practice; and the authors declare that they have no conflict of interest., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Several clinical studies have reported the analgesic effect of curcumin (Curc) in various situations such as rheumatoid arthritis, osteoarthritis, and postsurgical pain. Therefore, in this work, Curc-loaded electrospun nanofibers (NFs) are designed to evaluate their sustained release on analgesic effect duration in rats after epidural placement via repeated formalin and tail-flick tests. The Curc-loaded polycaprolactone/gelatin NFs (Curc-PCL/GEL NFs) are prepared through an electrospinning technique and introduced to the rat's epidural space after laminectomy. The physicochemical and morphology features of the prepared Curc-PCL/GEL NFs were characterized via FE-SEM, FTIR, and degradation assay. The in vitro and in vivo concentrations of Curc were measured to evaluate the analgesic efficacy of the drug-loaded NFs. Rat nociceptive responses are investigated through repeated formalin and tail-flick tests for 5 weeks after the placement of NFs. Curc had a sustained release from the NFs for 5 weeks, and its local pharmaceutical concentrations were much greater than plasma concentrations. Rat's pain scores in both early and late phases of the formalin test were remarkably decreased in the experimental period. Rat's tail-flick latency was remarkably enhanced and remained constant for up to 4 weeks. Our findings show that the Curc-PCL/GEL NFs can supply controlled release of Curc to induce extended analgesia after laminectomy., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Triple-negative breast cancer (TNBC) represents a challenging and aggressive form of breast cancer associated with limited treatment options and poor prognosis. Although chemotherapy is a primary therapeutic approach, drug resistance often hinders treatment success. However, the expanding knowledge of TNBC subtypes and molecular biology has paved the way for targeted therapies. Notably, exosomes (extracellular vesicles) have emerged as crucial carriers of tumorigenic factors involved in oncogenesis and drug resistance, facilitating cell-to-cell communication and offering potential as self-delivery systems. Among the cargo carried by exosomes, microRNAs (miRNAs) have gained attention due to their ability to mediate epigenetic changes in recipient cells upon transfer. Research has confirmed dysregulation of exosomal miRNAs in breast cancer cells compared to healthy cells, establishing them as promising biomarkers for cancer diagnosis and prognosis. In this comprehensive review, we summarize the latest research findings that underscore the diagnostic and prognostic significance of exosomal miRNAs in TNBC treatment. Furthermore, we explore contemporary therapeutic approaches utilizing these exosomal miRNAs for the benefit of TNBC patients, shedding light on potential breakthroughs in TNBC management., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Peptic ulcer disease (PUD) continues to be a cause of significant morbidity and mortality worldwide. Almost two-thirds of PUD cases are asymptomatic. In symptomatic patients, epigastric pain is the most common presenting symptom of PUD, which is manifested by nausea, abdominal fullness, bloating, and dyspepsia. Most PUD cases are associated with the use of COX inhibitors or Helicobacter pylori infection, or both. The traditional management of PUD includes the use of proton pump inhibitors to reduce the gastric acid secretion and antibacterial drugs to combat H. pylori. Timely diagnosis and treatment of PUD are vital to reduce the risk of associated morbidity and mortality, as is prevention of PUD among patients at high risk, including COX inhibitors users and those infected with H. pylori. PDE5 inhibitors have been used for the management of erectile dysfunction and pulmonary hypertension for decades. In recent years, studies have mentioned tremendous pleiotropic effects of PDE5 inhibitors on gastrointestinal, urogenital, musculoskeletal, reproductive, cutaneous, and neurologic disorders. Recent data shows that PDE5 inhibition augments gastric mucosa protection, and here, we review the most recent findings regarding the use of PDE5 inhibitors for the prevention and management of PUD., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Inflammatory bowel disease (IBD) is a chronic life-limiting disease of gastrointestinal tract characterized by widespread enteric inflammation. IBD is a multifactorial disease, and different environmental, microbial, and immune-related factors give rise to the development of disease. Among several factors, the preponderance of pro-inflammatory T helper 17 cells over the anti-inflammatory regulatory T cells augments inflammation in the intestinal mucosa. Prevailing evidence accentuates that PI3K signaling pathway plays a central role in the pathophysiology of the condition by regulating the inflammatory process in the gut mucosa. By recognizing the implications of PI3K in the pathogenesis of IBD, agents that could modulate this pathway have recently been at the focus of research, yielding encouraging results mainly in the experimental IBD models. In this review, we have summarized the recent advances, which may hold the keys to identify novel therapeutic strategies for IBD., (© 2023 Société Française de Pharmacologie et de Thérapeutique. Published by John Wiley & Sons Ltd.)

Lung cancer is one of the leading causes of death in both males and females, and it is the first causes of cancer-related deaths. Chemotherapy, surgery and radiotherapy are conventional treatment of lung cancer and recently, immunotherapy has been also appeared as another therapeutic strategy for lung tumor. However, since previous treatments have not been successful in cancer therapy and improving prognosis and survival rate of lung tumor patients, new studies have focused on gene therapy and targeting underlying molecular pathways involved in lung cancer progression. Nanoparticles have been emerged in treatment of lung cancer that can mediate targeted delivery of drugs and genes. Nanoparticles protect drugs and genes against unexpected interactions in blood circulation and improve their circulation time. Nanoparticles can induce phototherapy in lung cancer ablation and mediating cell death. Nanoparticles can induce photothermal and photodynamic therapy in lung cancer. The nanostructures can impair metastasis of lung cancer and suppress EMT in improving drug sensitivity. Metastasis is one of the drawbacks observed in lung cancer that promotes migration of tumor cells and allows them to establish new colony in secondary site. EMT can occur in lung cancer and promotes tumor invasion. EMT is not certain to lung cancer and it can be observed in other human cancers, but since lung cancer has highest incidence rate, understanding EMT function in lung cancer is beneficial in improving prognosis of patients. EMT induction in lung cancer promotes tumor invasion and it can also lead to drug resistance and radio-resistance. Moreover, non-coding RNAs and pharmacological compounds can regulate EMT in lung cancer and EMT-TFs such as Twist and Slug are important modulators of lung cancer invasion that are discussed in current review., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier Inc.)

Conjugated linoleic acids (CLAs) are polyunsaturated fatty acids primarily found in dairy products and ruminant animal products such as beef, lamb, and butter. Supplementation of CLAs has recently become popular among athletes due to the variety of health-promoting effects, including improvements in physical performance. Preclinical and some clinical studies have shown that CLAs can reduce inflammation and oxidative stress and favorably modulate body composition and physical performance; however, the results of previously published clinical trials are mixed. Here, we performed a comprehensive review of previously published clinical trials that assessed the role of CLAs in modulating inflammation, oxidative stress, body composition, and select indices of physical performance, emphasizing the molecular mechanisms governing these changes. The findings of our review demonstrate that the effect of supplementation with CLAs on inflammation and oxidative stress is controversial, but this supplement can decrease body fat mass and increase physical performance. Future well-designed randomized clinical trials are warranted to determine the effectiveness of (1) specific doses of CLAs; (2) different dosing durations of CLAs; (3) various CLA isomers, and the exact molecular mechanisms by which CLAs positively influence oxidative stress, inflammation, body composition, and physical performance., (© 2023. BioMed Central Ltd., part of Springer Nature.)

The article has been withdrawn at the request of the Corresponding author., Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused., The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.com/editorial-policies-main.php., Bentham Science Disclaimer: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Angiogenesis, the formation of new blood vessels, is an important stage in the growth of cancer. Extracellular matrix, endothelial cells, and soluble substances must be carefully coordinated during the multistep procedure of angiogenesis. Inducers and inhibitors have been found to control pretty much every phase. In addition to benign prostatic hyperplasia, prostatic intraepithelial neoplasia, and angiogenesis have a critical role in the initiation and progression of prostate cancer. MicroRNA (miRNA) is endogenous, short, non-coding RNA molecules of almost 22 nucleotides play a role in regulating cellular processes and regulating several genes' expression. Through controlling endothelial migration, differentiation, death, and cell proliferation, miRNAs have a significant function in angiogenesis. A number of pathological and physiological processes, particularly prostate cancer's emergence, depend on the regulation of angiogenesis. Investigating the functions played with miRNAs in angiogenesis is crucial because it might result in the creation of novel prostate cancer therapies that entail regulating angiogenesis. The function of several miRNAs and its targeting genes engaged in cancer of the prostate angiogenesis will be reviewed in this review in light of the most recent developments. The potential clinical utility of miRNAs potentially a novel therapeutic targets will also be explored, as well as their capacity to control prostate cancer angiogenesis and the underlying mechanisms., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Prostate carcinoma is a malignant situation that arises from genomic alterations in the prostate, leading to changes in tumorigenesis. The NF-κB pathway modulates various biological mechanisms, including inflammation and immune responses. Dysregulation of NF-κB promotes carcinogenesis, including increased proliferation, invasion, and therapy resistance. As an incurable disease globally, prostate cancer is a significant health concern, and research into genetic mutations and NF-κB function has the efficacy to facilitate the introduction of novel therapies. NF-κB upregulation is observed during prostate cancer progression, resulting in increased cell cycle progression and proliferation rates. Additionally, NF-κB endorses resistance to cell death and enhances the capacity for metastasis, particularly bone metastasis. Overexpression of NF-κB triggers chemoresistance and radio-resistance, and inhibition of NF-κB by anti-tumor compounds can reduce cancer progression. Interestingly, non-coding RNA transcripts can regulate NF-κB level and its nuclear transfer, offering a potential avenue for modulating prostate cancer progression., Competing Interests: Declaration of Competing Interest The authors declare no conflict of interest., (Copyright © 2023. Published by Elsevier Ltd.)

MicroRNA-126 (miR-126) has become a key player in the biology of cancer, playing a variety of functions in carcinogenesis and cancer development. The diagnostic and prognostic potential of miR-126 in diverse cancer types is summarized in this thorough analysis, with an emphasis on its role in tumor angiogenesis, invasion, metastasis, cell proliferation, apoptosis, and treatment resistance. MiR-126 dysregulation is linked to a higher risk of developing cancer and a worse prognosis. Notably, miR-126 affects tumor vascularization and development by targeting vascular endothelial growth factor-A (VEGF-A). Through its impact on genes involved in cell adhesion and migration, it also plays a vital part in cancer cell invasion and metastasis. Additionally, miR-126 controls drug resistance, apoptosis, and cell proliferation, which affects cancer cell survival and treatment response. It may be possible to develop innovative therapeutic approaches to stop tumor angiogenesis, invasion, and metastasis, as well as combat drug resistance by focusing on miR-126 or its downstream effectors. The versatility of miR-126's functions highlights the role that it plays in cancer biology. To understand the processes behind miR-126 dysregulation, pinpoint precise targets, and create efficient therapies, more investigation is required. Utilizing miR-126's therapeutic potential might have a significant influence on cancer treatment plans and patient outcomes., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Cholangiocarcinoma, also referred to as CCA, is a highly complex epithelial malignancy that can impact various organs and regions of the body, including the perihilar, intrahepatic, and distal organs. This cancer is characterized by the malignant growth of the epithelial lining in the bile ducts, which spans the entire biliary tree and is accountable for disease progression. The current state of affairs concerning CCA is concerning, with poor prognoses, high recurrence rates, and dismal long-term survival rates significantly burden healthcare facilities worldwide. Studies have identified numerous signaling pathways and molecules involved in the development and progression of CCA, including microRNAs, an important class of non-coding RNAs that have the ability to modulate these cellular signaling pathways significantly. In addition, microRNAs may serve as an innovative target for developing novel therapeutic approaches for CCA. In this review, we explore the underlying mechanisms and signaling pathways implicated in the initiation and progression of CCA, focusing on the future direction of utilizing microRNAs as a promising treatment option for this challenging malignancy., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Although photothermal treatment (PTT) has made significant progress in the fight against cancer, certain types of malignant tumors are still difficult to eradicate. PTT uses photothermal transforming agents to absorb NIR light and convert it to thermal energy, causing cancer cell death. In this study, we synthesized alginate (Alg)-coated CuS nanoparticles (CuS@Alg) as photothermal transforming agents to kill glioblastoma cancer cells. Nanoparticles were synthesized via a facile method, then, were characterized with different techniques such as ultraviolet-visible spectroscopy (UV-Vis), Fourier transform infrared (FTIR), X-ray diffraction analysis (XRD), transmission electron microscopy (TEM), and dynamic light scattering (DLS). Nanoparticles show high stability, and are monodisperse. CuS@Alg was discovered to have a spherical shape, a hydrodynamic size of about 19.93 nm, and a zeta potential of - 9.74 mV. CuS@Alg is able to increase temperature of medium under NIR light. Importantly, in vitro investigations show that PTT based on CuS@Alg has a strong theraputic impact, resulting in much high effectiveness. The LD50 and histopathology assays were used to confirm the NPs' non-toxicity in vivo. Results from an in vivo subacute toxicity investigation showed that the fabricated NPs were perfectly safe to biomedical usage., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Natural killer (NK) cells are innate immune cells with cytotoxic potentials to kill cancerous cells in several mechanisms, which could be implied for cancer therapy. While potent, their antitumor activities specially for solid tumors impaired by inadequate tumor infiltration, suppressive tumor microenvironment, cancer-associated stroma cells, and tumor-supportive immune cells. Therefore, manipulating or reprogramming these barriers by prospective strategies might improve current immunotherapies in the clinic or introduce novel NK-based immunotherapies. NK-based immunotherapy could be developed in monotherapy or in combination with other therapeutic regimens such as oncolytic virus therapy and immune checkpoint blockade, as presented in this review., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Management of cancer metastasis has been associated with remarkable reduction in progression of cancer cells and improving survival rate of patients. Since 90% of mortality are due to cancer metastasis, its suppression can improve ability in cancer fighting. The EMT has been an underlying cause in increasing cancer migration and it is followed by mesenchymal transformation of epithelial cells. HCC is the predominant kind of liver tumor threatening life of many people around the world with poor prognosis. Increasing patient prognosis can be obtained via inhibiting tumor metastasis. HCC metastasis modulation by EMT and HCC therapy by nanoparticles are discussed here. First of all, EMT happens during progression and advanced stages of HCC and therefore, its inhibition can reduce tumor malignancy. Moreover, anti-cancer compounds including all-trans retinoic acid and plumbaging, among others, have been considered as inhibitors of EMT. The EMT association with chemoresistance has been evaluated. Moreover, ZEB1/2, TGF-β, Snail and Twist are EMT modulators in HCC and enhancing cancer invasion. Therefore, EMT mechanism and related molecular mechanisms in HCC are evaluated. The treatment of HCC has not been only emphasized on targeting molecular pathways with pharmacological compounds and since drugs have low bioavailability, their targeted delivery by nanoparticles promotes HCC elimination. Moreover, nanoparticle-mediated phototherapy impairs tumorigenesis in HCC by triggering cell death. Metastasis of HCC and even EMT mechanism can be suppressed by cargo-loaded nanoparticles., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Ali G. Alkhathami reports was provided by King Khalid University., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Osteoarthritis (OA) is the most common type of arthritis. Its high prevalence, especially in the elderly, and its negative impact on physical function make it a leading cause of disability in the elderly. Joint pain as well joint stiffness are the common classic signs of OA. Chondrocyte death together with loss of articular cartilage integrity are the main pathologic changes in OA. Non-steroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids are commonly used for the management of OA; still, their effectiveness is limited, and no therapeutic strategy is able to fully stop OA progression. Ferroptosis is a kind of cell death, distinct from apoptosis and necroptosis, caused by iron-dependent peroxidation of membrane phospholipids that terminates cell life by disintegrating all plasma membranes. It has been suggested that ferroptosis has a critical role in decreased viability of chondrocytes in OA, and here, we review recent findings regarding the pathologic pathways that lead to chondrocyte ferroptosis, and discuss the possible therapeutic utility of ferroptosis inhibition in OA., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Objectives: Diabetic neuropathic pain (DNP) is a debilitating symptom of diabetic neuropathy which seriously impairs patient's quality of life. Currently, there is no specific therapy for DNP except for duloxetine and gabapentin that show limited utility in alleviating DNP. The present review aims to discuss the central role of protein kinases in the pathogenesis of DNP and their therapeutic modulation., Methods: Scopus, PubMed, and Google scholar were searched up to January 2022 to find relevant studies with English language in which the roles of proteins kinases in DNP were examined., Results: DNP is associated with hyperactivity in pain sensory neurons and therapies aim to specifically suppress redundant discharges in these neurons without affecting the activity of other sensory and motor neurons. Transient receptor potential vanilloid 1 (TRPV1) and purinergic 2 × 7 receptors (P2 × 7R) are two receptor channels, highly expressed in pain sensory neurons and their blockade produces remarkable analgesic effects in DNP. The activities of receptor channels are mainly regulated by the protein kinases whose modulation provides remarkable analgesic effects in DNP models., Conclusion: Capsaicin, TRPV1 modulator, is the only agent successfully examined in clinical trials with promising effects in patients with DNP. Current data suggest that blocking calcium calmodulin dependent protein kinase II (CaMKII) is superior to other approaches, considering its pivotal role in regulating the pain neuron potentials. By this means, DNP alleviation is achievable without affecting the activity of other sensory or motor neurons., Competing Interests: Competing InterestsThe authors have no relevant financial or non-financial interests to disclose., (© The Author(s), under exclusive licence to Tehran University of Medical Sciences 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.)

Background and Aims: Several randomized controlled trials (RCTs) have shown that almonds can improve oxidative stress indices, but the results are controversial. Therefore, the goal of this research was to carry out a systematic review and meta-analysis of all RCTs that evaluated the effect of almonds on selected oxidative stress indices., Methods: A systematic search was conducted up to April 2022 on PubMed, Scopus, Web of Science, and Google Scholar. We have selected the studies that investigated the effects of almonds on malondialdehyde (MDA), and oxidized low-density lipoprotein (Ox-LDL) levels in adults. Data were pooled by using the random-effects model. The risk of bias in individual studies was assessed using the Cochrane Collaboration risk of bias tool., Results: Seven RCTs involving 424 participants were analyzed. The results indicated that almond intake led to a significant decrease in MDA levels (WMD: - 6.63 nmol/ml; 95 % CI: - 8.72 to - 4.54; P < 0.001). However, no significant effect was observed on Ox-LDL (Hedges' g: - 0.12; 95 % CI: - 0.34 to 0.10; P = 0.28). Sensitivity analysis showed that overall estimates were not affected by the elimination of any study. We did not observe any evidence regarding publication bias., Conclusion: The present meta-analysis suggests that almond intake can improve MDA levels and might play a beneficial role in the reinforcement of the antioxidant defense system and amelioration of oxidative stress in adults. There is a need for more studies with larger groups to better estimate this effect., Competing Interests: Conflict of interest The authors declare that they have no conflict of interest., (Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with a poor prognosis which is lethal in over 90% of cases despite the standard therapies. Mainly activated by Janus kinase 2 (JAK2), signal transducer and activator of transcription 3 (STAT3) is a key transcription factor, capable of exerting the expression of multitude of genes involved in survival. Moreover, STAT3 activity is regulated by the interleukin 28 receptor α (IL28RA) and glutathione s-transferase mu-3 (GSTM3), up-regulation of both contributes to the invasiveness of pancreatic cancer cells. In this regard, STAT3 overactivity has an important pathogenic role in the development of PDAC as it is associated with enhanced cell proliferation, survival, angiogenesis, and metastasis. STAT3-associated expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinase 3 and 9 are implicated in the angiogenic and metastatic behavior of the PDAC. Multitude of evidence underline the protective role of STAT3 inhibition against PDAC both in cell cultures and in tumor grafts. However, specific inhibition of STAT3 was not feasible until recently, when a selective potent chemical STAT3 inhibitor, termed N4, were developed and it turned out to be highly effective against PDAC in vitro, as well as in vivo. This review aims to discuss the most recent advances in our understanding of STAT3 role in the pathogenesis of PDAC and its therapeutic applications., Competing Interests: Conflict of interest The authors have no relevant financial or non-financial interests to disclose., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Diseases or defects of the skeleton are hazardous because of their specificity and intricacy. Bone tissue engineering has become an important area of research that offers promising new tools for making biomimetic hydrogels that can be used to treat bone diseases. New hydrogels with a distinctive 3D network structure, high water content, and functional capabilities are ranked among the most promising candidates for bone tissue engineering. This makes them helpful in treating cartilage injury, skull deformity, and arthritis. This review will briefly introduce the variety of biocompatible functional hydrogels used in cell culture and bone tissue regeneration. Many gel design concepts, such as crosslinking procedures, controlled release properties, and alternative bionic methodology, were stressed regarding injectable hydrogels to form bone tissue. Hydrogels manufactured from biocompatible materials are a promising option for minimally invasive surgery because of their adaptable physicochemical qualities, ability to fill irregularly shaped defect sites, and ability to grow hormones or release drugs in response to external stimuli. Also included in this overview is a quick rundown of the more practical designs employed in treating bone disorders. Essential details on injectable hydrogel scaffolds for bone tissue regeneration are described in this article., Competing Interests: Competing interestsThe authors declare no competing interests., (© International Union for Pure and Applied Biophysics (IUPAB) and Springer-Verlag GmbH Germany, part of Springer Nature 2023, Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.)

Caries is the most prevalent and widespread chronic oral disease. Traditional caries filling materials, due to their lack of anti-caries capabilities, can readily develop secondary caries. Nanomaterials proposed as an effective approach for caries treatment can inhibit biofilm formation. It also can not only reduce demineralization but also promote remineralization. In recent years, nanotechnology in anti-caries materials, particularly nano-adhesive and nano-composite resin, has advanced rapidly. Because inorganic nanoparticles (NPs) interfere with bacterial metabolism and inhibit biofilm development, inorganic NPs have emerged as a new trend in dental applications. Metal and metal oxide NPs by releasing metal ions, oxidative stress induction, and non-oxidative mechanisms showed significant antimicrobial activity. For applying metal and metal oxide NPs as anti caries agents, silver, zinc, titanium, copper, and calcium ions have been shown significant attention. Moreover, fluoride functionalized inorganic NPs were also employed to improve their efficacy of them. The fluoride-functionalized NPs can promote remineralization, and inhibit demineralization by enhancing apatite formation. In this review, we have provided an overview and recent advances in the use of inorganic NPs as anti caries agents. Furthermore, their antimicrobial, remineralizing, and mechanical impacts on dental materials were discussed., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2023 The Authors.)

Objectives: Breast cancer is the most prevalent cancer among females with different molecular subtypes. Corosolic acid is a pentacyclic triterpenoid with anti-cancer properties., Materials and Methods: The MTT assay was used to assess the cytotoxic activity of corosolic acid on MDA-MB-231 and MCF7 cell lines. To determine the apoptotic cells, the flow cytometry technique was utilized. The expression levels of apoptosis-related genes and proteins were quantified using quantitative real time-PCR (qRT-PCR) and Western blotting methods. The activity of caspase enzymes was measured by spectrophotometry., Results: Corosolic acid significantly inhibited the proliferation of both cell lines compared with controls. This agent markedly induced apoptosis in MDA-MB-231 cells but did not affect MCF7 cells compared with controls. Treating the MADA-MB-231 and MCF7 cell lines with corosolic acid showed an inducing effect on apoptosis-associated caspases, including Caspase-8, 9, and -3, in MADA-MB-231 cells with no effect on apoptotic markers in MCF7 cells. Further experiments uncovered corosolic acid-induced apoptosis in MADA-MB-231 cells by decreasing the expression of the phosphorylated form of JAK2 and STAT3 proteins., Conclusion: The present data suggested that corosolic acid is an apoptosis-inducing phytochemical in triple-negative breast cancer MADA-MB-231 cells. Also, corosolic acid triggered apoptosis in these cells by stimulating both pathways of apoptosis and inhibiting the JAK/STAT signaling. Furthermore, corosolic acid was found to inhibit MCF7 cell proliferation by a non-apoptotic mechanism., Competing Interests: The authors have no conflicts of interest to declare.

The main objective of the current study is to fabricate a 3D scaffold using alginate hydrogel implemented with carbon nanoparticles (CNPs) as the filler. The SEM imaging revealed that the scaffold possesses a porous internal structure with interconnected pores. The swelling value of the scaffolds (more than 400%) provides a wet niche for bone cell proliferation and migration. The in vitro evaluations showed that the scaffolds were hemocompatible (with hemolysis induction lower than 5%) and cytocompatible (inducing significant proliferative effect (cell viability of 121 ± 4%, p < 0.05) for AlG/CNPs 10%). The in vivo studies showed that the implantation of the fabricated 3D nanocomposite scaffolds induced a bone-forming effect and mediated bone formation into the induced bone defect. In conclusion, these results implied that the fabricated NFC-integrated 3D scaffold exhibited promising characteristics beneficial for bone regeneration and can be applied as the bone tissue engineering scaffold., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Nowadays, the most common approaches in the prognosis, diagnosis, and treatment of diseases are along with undeniable limitations. Thus, the ever-increasing need for using biocompatible natural materials and novel practical modalities is required. Applying biomaterials, such as chitosan nanoparticles (CS NPs: FDA-approved long-chain polymer of N-acetyl-glucosamine and D-glucosamine for some pharmaceutical applications), can serve as an appropriate alternative to overcome these limitations. Recently, the biomedical applications of CS NPs have extensively been investigated. These NPs and their derivatives can not only prepare through different physical and chemical approaches but also modify with various molecules and bioactive materials. The potential properties of CS NPs, such as biocompatibility, biodegradability, serum stability, solubility, non-immunogenicity, anti-inflammatory properties, appropriate pharmacokinetics and pharmacodynamics, and so forth, have made them excellent candidates for biomedical applications. Therefore, CS NPs have efficiently applied for various biomedical applications, like regenerative medicine and tissue engineering, biosensors for the detection of microorganisms, and drug delivery systems (DDS) for the suppression of diseases. These NPs possess a high level of biosafety. In summary, CS NPs have the potential ability for biomedical and clinical applications, and it would be remarkably beneficial to develop new generations of CS-based material for the future of medicine., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Introduction: This paper sought to scrutinize the role of microRNA-32 (miR-32) on the growth and migration as well as on the expression of metastatic genes in PC3 cells of prostate cancer in vitro., Methods: Subsequent transfection of cells with miR-32 mimics, miR-32 inhibitor, negative control (NC), cell proliferation using MTT, and apoptosis by ELISA were performed. Furthermore, qRT-PCR was directed to measure the expression levels of matrix metalloproteinase 2 (MMP2) and vascular endothelial growth factors (VEGF) as metastatic and angiogenesis genes in the progression of PC3., Results: miR-32 was overexpressed in PC3 cells compared to normal cells ( P <0.001). Down-regulation of miR-32 obstructs in vitro proliferation and migration while intensifying the apoptosis rate in PC3 cells. Also, we found that miR-32 negatively modulates the expression of VEGF and MMP2 in PC3 cells., Conclusion: These results indicate that the suppression of miR-32 might offer an auxiliary treatment procedure for addressing the invasion, progression, and metastasis in PCa patients by improving cell apoptosis., Competing Interests: The authors declare that they have no conflict of interest., (Thieme. All rights reserved.)

Autophagy is defined as a "self-digestion" signal, and it is a cell death mechanism its primary function is degrading toxic agents and aged organelles to ensure homeostasis in cells. The basic leve ls of autophagy are found in cells, and when its levels exceed to standard threshold, cell death induction is observed. Autophagy dysregulation in cancer has been well-documented, and regulation of this pathway by epigenetic factors, especially microRNAs (miRNAs), is interesting and noteworthy. miRNAs are considered short endogenous RNAs that do not encode functional proteins, and they are essential regulators of cell death pathways such as apoptosis, necroptosis, and autophagy. Accumulating data has revealed miRNA dysregulation (upregulation or downregulation) during tumor progression, and their therapeutic manipulation provides new insight into cancer therapy. miRNA/autophagy axis in human cancers has been investigated an exciting point is the dual function of both autophagy and miRNAs as oncogenic and onco-suppressor factors. The stimulation of pro-survival autophagy by miRNAs can increase the survival rate of tumor cells and mediates cancer metastasis via EMT inductionFurthermore, pro-death autophagy induction by miRNAs has a negative impact on the viability of tumor cells and decreases their survival rate. The miRNA/autophagy axis functions beyond regulating the growth and invasion of tumor cells, and they can also affect drug resistance and radio-resistance. These subjects are covered in the current review regarding the new updates provided by recent experiments., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Endometriosis is a chronic gynecologic disorder characterized by abnormal growth of endometrium-like tissues in the ectopic regions of the pelvic peritoneum. The pathophysiology of endometriosis is not completely understood; however, excessive endometrial cell proliferation together with resistance to apoptosis facilitates the migration, implantation, and survival of endometrial cells in the distant sites. Endoplasmic reticulum (ER) stress response (also called unfolded protein response) is a cellular defense mechanism triggered by ER stress. When severe enough, the so-called response initiates cell suicide, i.e., apoptosis. Therefore, therapeutic induction of ER stress in endometriotic cells could promote apoptosis and contribute to the management of disease. In this review, we discuss the pathogenic role of ER stress in endometriosis and the most recent findings regarding the induction of ER stress in connection with endometriosis., (© 2023. The Author(s), under exclusive licence to Cell Stress Society International.)

Exposure to polycyclic aromatic hydrocarbons (PAHs) during pregnancy has been associated with many adverse child health. However, the evidence on such associations with child brain development was not reviewed systemically. Therefore, in this study, we systemically reviewed the observational studies on prenatal exposure to PAHs and childhood intelligence quotient (IQ). The Meta-analyses Of Observational Studies in Epidemiology (MOOSE) guidelines were applied to perform this review. We systematically searched Scopus, PubMed, and Web of Science for all relevant articles published in English until 15 October 2022. The quality of retrieved studies was evaluated based on the Gascon et al. method. We retrieved a total of 351 citations through the initial search, of which an overall of six articles ([Formula: see text] participants) were included in our final review. The quality assessment indicated that four studies had excellent and two studies had good quality. Three reviewed studies reported a significant negative association between prenatal exposure to PAHs and children's IQ. One study reported that exposure to PAHs combined with material hardship was associated with lower child IQ and one study indicated lower child IQ through lower LINE1 DNA methylation-related maternal exposure to PAHs. However, another study did not observe a significant association between prenatal PAH exposure and child IQ. Overall, our review indicated that exposure to PAHs during pregnancy has an adverse impact on childhood IQ., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Background: The role of screen time in promoting obesity among children has been reported in previous studies. However, the effects of different screen types and the dose-response association between screen time and obesity among children is not summarized yet. In the current meta-analysis we systematically summarized the association between obesity and screen time of different screen types in a dose-response analysis., Methods: A systematic search from Scopus, PubMed and Embase electronic databases was performed. Studies that evaluated the association between screen time and obesity up to September 2021 were retrieved. We included 45 individual studies that were drawn from nine qualified studies into meta-analysis., Results: The results of the two-class meta-analysis showed that those at the highest category of screen time were 1.2 times more likely to develop obesity [odds ratio (OR) = 1.21; confidence interval (CI) = 1.113, 1.317; I 2  = 60.4%; P < 0.001). The results of subgrouping identified that setting, obesity status and age group were possible heterogeneity sources. No evidence of non-linear association between increased screen time and obesity risk among children was observed (P-nonlinearity = 0.310)., Conclusion: In the current systematic review and meta-analysis we revealed a positive association between screen time and obesity among children without any evidence of non-linear association. Due to the cross-sectional design of included studies, we suggest further studies with longitudinal or interventional design to better elucidate the observed associations., (© 2023. The Author(s).)

This study aimed to evaluate the potential of mesenchymal stem cell-derived exosomes loaded with curcumin (Curc-Exos) as an effective therapeutic strategy for rheumatoid arthritis through modulation of proliferation and inflammatory response in HIG-82 synovial cells. For this purpose, Exos were isolated and characterized with BCA protein assay, DLS, FE-SEM, and TEM. The Curc was embedded by mixing it with Exos in a 1:4 ratio. It was found that the Curc stability has improved after loading on Exos compared to the free Curc. Besides, the in vitro studies using LPS-stimulated HIG-82 synovial cells indicated the efficiency of Curc-Exos in enhancing cytotoxicity and apoptosis compared to the free Curc treatment. It was also revealed that Curc-Exos significantly could reduce the expression levels of anti-apoptotic proteins IAP1 and IAP2 and inflammatory mediators including IL-6, TNF-α, MMP1, and PGE2. This preliminary study confirmed the suitability of Curc-Exos in counteracting the proliferation and inflammatory response of rheumatoid arthritis synovial fibroblasts in vitro., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Before very sensitive current genomics platforms were discovered, long non-coding RNAs (lncRNAs) as controllers of gene expression, were thought to be accumulated genetic garbage. The past few years have seen a lot of interest in a large classification of non-coding transcripts with an indeterminate length of more than 200 nucleotides [1]. lncRNAs' association with immunity and disease progression has been revealed by a growing body of experimental research. Only a limited subset of lncRNAs, however, has solid proof of their role. It is also clear that various immune cells express lncRNAs differently. In this review, we concentrated on the role of lncRNA expression in the regulation of immune cell function and response to pathological conditions in macrophages, dendritic cells, natural killer (NK) cells, neutrophils, Myeloid-derived suppressor cells (MDSCs), T cells, and B cells. The innate and adaptive immune response systems may be significantly regulated by lncRNAs, according to emerging research. To discover possible therapeutic targets for the therapy of different diseases, it may be helpful to have a better realization of the molecular mechanisms beyond the role of lncRNAs in the immune response. Therefore, it is crucial to investigate lncRNA expression and comprehend its significance for the immune system., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Nanomaterials and nanostructures have shown fascinating performances in various biomedicine fields, from cosmetic to cancer diagnosis and therapy. Engineered nanomaterials can encapsulate both lipophilic and hydrophilic substances/drugs to eliminate their limitations in the free forms, such as low bioavailability, multiple drug administration, off-target effects, and various side effects. Moreover, it is possible to deliver the loaded cargo to the desired site of action using engineered nanomaterials. One approach that has made nanocarriers more sophisticated is the "biomimetic" concept. In this scenario, biomolecules (e.g., natural proteins, peptides, phospholipids, cell membranes) are used as building blocks to construct nanocarriers and/or modify agents. For instance, it has been reported that specific cells tend to migrate to a particular site during specific circumstances (e.g., inflammation, tumor formation). Employing the cell membrane of these cells as a coating for nanocarriers confers practical targeting approaches. Accordingly, we introduce the biomimetic concept in the current study, review the recent studies, challenge the issues, and provide practical solutions., Competing Interests: Conflict of interestThe authors declare no competing interests., (© Qatar University and Springer Nature Switzerland AG 2023, Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.)

Breast cancer (BC) is both an inherited and environmental-based disease which is the leading cause of death among women. Early detection of BC can prevent invasion and metastasis in patients. Currently, researchers endeavor to find non-invasive biological markers from body fluids. Circulating non-coding RNAs such as microRNAs (miRNAs) can potentially be valuable prognostic and detective biomarkers. To identify novel miRNA-based biomarkers, we utilized bioinformatic tools. To reach this goal, the miRNA expression profiles of GSE31309, GSE 44,281, GSE98181, and GSE118782 were analyzed through a limma package of R. Target gene prediction of differentially expressed miRNAs, called differentially expressed miRNAs (DEMs), between samples of healthy individuals and BC patients was implemented through Multimir package of R. Functional enrichment analysis of predicted target genes through Enrich R (online database) revealed that most of the genes are enriched in the mitochondrial outer membrane for cellular component, intrinsic apoptotic signaling regulations for biological processes, transcription co-receptor activity for molecular functions, and dopaminergic synapse pathway. Furthermore, our survival analysis results revealed that miR-29c and mir-361 have the potential to serve as prognostic biomarkers., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Background: Although radiotherapy is one of the main cancer treatment modalities, exposing healthy organs/tissues to ionizing radiation during treatment can lead to different adverse effects. In this regard, it has been shown that the use of radioprotective agents may alleviate the ionizing radiation-induced toxicities., Objective: The present study aims to review the radioprotective potentials of silymarin/silibinin in the prevention/reduction of ionizing radiation-induced adverse effects on healthy cells/tissues., Methods: Based on PRISMA guidelines, a comprehensive and systematic search was performed for identifying relevant literature on the "potential protective role of silymarin/silibinin in the treatment of radiotherapy-induced toxicities" in the different electronic databases of Web of Science, PubMed, and Scopus up to April 2022. Four hundred and fifty-five articles were obtained and screened in accordance with the inclusion and exclusion criteria of the current study. Finally, 19 papers were included in this systematic review., Results: The findings revealed that the ionizing radiation-treated groups had reduced survival rates and body weight in comparison with the control groups. It was also found that radiation can induce mild to severe adverse effects on the skin, digestive, hematologic, lymphatic, respiratory, reproductive, and urinary systems. Nevertheless, the administration of silymarin/silibinin could mitigate the ionizing radiation-induced adverse effects in most cases. This herbal agent exerts its radioprotective effects through anti-oxidant, anti-apoptosis, anti-inflammatory activities, and other mechanisms., Conclusion: The results of the current systematic review showed that co-treatment of silymarin/silibinin with radiotherapy alleviates the radiotherapy-induced adverse effects in healthy cells/tissues., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

The incidence of cancer has been growing worldwide. Better survival rates following the administration of novel drugs and new combination therapies may concomitantly cause concern regarding the long-term adverse effects of cancer therapy, for example, second primary malignancies. Moreover, overcoming tumour resistance to anticancer agents has been long considered as a critical challenge in cancer research. Some low toxic adjuvants such as herb-derived molecules may be of interest for chemoprevention and overcoming the resistance of malignancies to cancer therapy. Apigenin is a plant-derived molecule with attractive properties for chemoprevention, for instance, promising anti-tumour effects, which may make it a desirable adjuvant to reduce genomic instability and the risks of second malignancies among normal tissues. Moreover, it may improve the efficiency of anticancer modalities. This paper aims to review various effects of apigenin in both normal tissues and malignancies. In addition, we explain how apigenin may have the ability to protect usual cells against the genotoxic repercussions following radiotherapy and chemotherapy. Furthermore, the inhibitory effects of apigenin on tumours will be discussed., (© 2022 John Wiley & Sons Australia, Ltd.)